Dental Mgmt: Diabetes Flashcards
Diabetes can result from a combo of defects in both:
insulin secretion and action
Diabetes affects the metabolism of what type of nutrient(s)?
every type (carbs, fats, proteins)
NIDDM sf:
Non-insulin dependent diabetes
What does the body use if it cant’ use glucose?
FA –> ketoacidosis
The use of FA for energy can lead to:
ketoacidosis, triglycerides –> FA’s –> fuel source
How does insulin maintain glucose homeostasis:
promoting glucose uptake into cells and storage in liver as glycogen
Insulin promotes the uptake of these:
glucose, FA’s and AA’s
TF? Cells can not use glucose as an energy source in diabetes.
T
How does Type 1 diabetes affect insulin levels?
AI destruction of pancreatic B cells
% of ppl w Type 2:
90%-95%
Typical age for the onset of Type 1 diabetes:
15yo
Pts w Type 1 are more prone to have:
Grave’s, Addison’s, Hashimoto’s
TF? Some pts w DM have no evidence of autoimmunity.
T
What’s impaired in Type 2?
insulin function
Typically age of onset for type 2 diabetes:
40+, lower every yr
TF? Only minor Beta cell destruction in Type 2.
F. none
Is ketoacidosis more common in Type 1 or 2?
1, rare in Type 2
Types of diabetes:
AI, Type 2, gestational, pancreatic tumor, steroid induced, MRDM (malnutrition related DM), viral?
TF? Gestational DM usually stays w a woman after birth.
F. USUALLY goes away.
TF? Women are more predisposed to Type 2 DM later in life if they get gestational during pregnancy.
T
Ppl in US w diabetes.
29 million (8million undiagnosed)
% of pop in US w DM:
9.3%
% pop over 65yo w DM:
26%
of ppl w pre-diabetes:
86million and growing
Pre-diabetic range, mg/dl:
100 - 126
Diabetic, mg/dl:
126+
Normal, mg/dl::
under 100
Risk factors for Type 2:
age, obesity, genetics, insulin resistant muscle, fat, and liver cells, abnormal liver glucose production, elevated glucagon levels
Diabetics are __ times more likely to develop CV disease.
2
Diabetics are __ times more likely to have necrosis of extremities:
5
Diabetics are __ times more likely to have renal failure:
17
Diabetics are __ times more likely to go blind:
25
TF? Insulin resistance is related to high cerebral glucose.
F. low
TF? Insulin resistance is related to an inc risk of Alzheimer’s dementia.
T
How does high fructose corn syrup affect a persons body?
alters metabolism
2 episodes of hypoglycemia increases a persons risk of developing dementia how many times?
2X
Vascular complications in diabetes results from:
microangiopathy and atherosclerosis
Where do vascular changes occur in the body?
throughout
Where are vascular changes most damaging in the body?
kidney and retina, brittle vessels
Molecular level changes that lead to vascular complications:
accumulation of polyols, adv glycation end products, inc VEGF, lipid deposition
Oral manifestations of vascular complications:
xerostomia, infection, poor healing, inc caries, gingival and perio problems, candidiasis, burning mouth, soft/hard tissue changes, bony changes
Main complaint of diabetics:
dry mouth
What does the dry mouth result from?
systemic dehydration, altered salivary flow, meds, autonomic dysfunction, altered BM of glands, fatty deposits in parotid gland (seen in HIV pts too)
How is the viscosity of saliva altered w fat deposition?
increased viscosity
How is the parotid gland affected by fat deposition?
enlarges
Effects of xerostomia:
caries (not pit and fissure), altered taste, burning mouth, discomfort, inability to swallow if severe
Diabetic neuropathy may lead to:
burning, tingling, numbness, pain
How to red oral burning and taste disturbances:
good diabetic control
Taste sense most likely to be affected by DM:
sweet, disordered glucose receps
TF? Burning mouth syndrome is not really a syndrome.
T
Types of burning mouth:
1’ or 2’
Which is idiopathic, 1’ or 2’?
1’
Burning mouth can be secondary to:
xerostomia, candidiasis, anxiety, depression, GERD, endocrine disorders, hormonal imbalance, esp. menopause, diabetes, hypothyroidism, nutritional deficiencies, esp Vit B, ZInc, Folate, and iron
Ppl more likely to have a raw, depapillated tongue:
post menopausal, take blood glucose
Soft tissue changes that an occur:
exaggerated gingival response to plaque, similar to pregnancy gingivitis, hyperplastic, erythematous gingiva, acute gingival abscesses
A hyperplastic growth could be due to:
DM
1st identifiable oral manifestation of DM:
dramatic, aggressive pdd at a young age
Pts w DM are more prone to these as a result of periodontitis:
acute gingival abscess (tartar of food in pseudopocket)
How does DM promote periodontitis?
exaggerated inflammatory response to microflora
Are gingival crevicular fluid levels of glucose inc or dec in pts w DM?
inc
Effect of high gingival crevicular fluid levels of glucose:
changes interactions bw cells and their ECM in periodontium, good env for bad bacteria, inc production of end stage products
AGE sf:
Advanced Glycation End-products
What are AGE:
damaged proteins that accumulate and cause tissue damage
AGE bind to:
mac and monocyte receptors and inc secretion of interleukin-1 & TNF-alpha- tissue destruction
What does AGE formation results in?
collagen build up in capillary basement membranes, dec perfusion, tissue destruction, dec ability to repair, inc risk of infection
Immunological changes:
dec wound healing, inc risk of infection, infection more likely to have severe sequelae
How to treat infections w DM pts?
aggressively, includes periodontitis
What causes dec wound healing?
Red phagocytic activity, delayed chemotaxis, vascular changes, abnormal collagen production, genetics, 1’ relative have some defects in collagen production wo having DM (may be familial component)
Why is an inflammatory response dec in extremities of pts w DM?
brittle vasculature
Immunological changes are related to
immune status, inc risk for candidiasis & other fungal infections
Fungal infections can lead to:
xerostomia, inc salivary glucose levels, immune effects
Fungal infections of the mouth:
candidiasis, angular cheilitis
When is angular cheilitis more common?
winter, dec VD
When to assume a fungal infection is systemic:
if you can’t see where infection stops in oral cavity, dangerous
How to treat hyperplastic candidiasis
debride, medicate
What does it mean if infection stops at denture line?
denture is infected, not as dangerous as systemic
How to treat fungal infection that stops at denture line:
topically
Issue w Rxing topicals to treat fungal infection:
pt compliance, pt thinks that are healed when they are not and should continue taking but they don’t and get reinfected
Mucosal mycosis:
fungal infection, AIDS, poorly controlled DM, starts as sinus or nasal infection, can perforate to OC
Tx duration of oral candidiasis:
2wks for all
2 tx for oral candidiasis that are dissolved in mouth:
topical clotrimazole (5X/d), nystatin suppositories (6-8X/d)
2 txs for oral candidiasis that are treated w 100mg and 200mg/d respectively:
Systemic Fluconazole, systemic ketoconazole
Rhinocerebral Mucomycosis
Fungal infection caused mainly by Rhizopus oryzae, high risk of infection in those with DKA, presents as fever, nasal pain, ulceration, and necrosis with black nasal discharge, can spread quickly to brain
Tx for Rhinocerebral Mucomycosis:
surgical debridement of tissues & intravenous lipid formulation amphotericin B starting at 5mg/kg/d w some doctors inc dose to 10mg/kg/d, control predisposing factors contributing to infection: hyperglycemia, metabolic acidosis
DKA sf:
diabetic ketoacidosis
a group of fungi that cause Rhinocerebral Mucormycosis:
Mucorales, mainly Rhizopus oryzae
Does Rhinocerebral Mucormycosis have a high or low mortality rate?
high
Pts most susceptible to Rhinocerebral Mucormycosis:
DM, immunocompromised
What property of the fungus puts those with diabetic ketoacidosis at higher risk?
an enzyme that allows them to grow in a hyperglycemic, acidic conditions
How are patients infected w Rhinocerebral Mucormycosis?
Spores inhaled through nose or lungs
Presentation of Rhinocerebral Mucomycosis:
fever, congestion, pain, ulceration, necrosis, bloody or black nasal discharge, facial or periorbital swelling, dec vision &/ or double vision.
There MIGHT be an inc incidence of this in pts w DM:
atrophic and erosive forms of lichen planus
Which has a more sig inc in atrophic and erosive forms of lichen planus, Type 1 or 2?
Type 1
What predisposes pts w Dm to oral infections?
poor control of it
What dental tx, if any, can we do for well-controlled diabetics who lack secondary manifestations such as renal disease and cardiovascular involvement?
all indicated dental tx
ASA categorization of well controlled DM:
ASA 2
how to treat pts w medically compromising conditions
compromised treatment plans, more aggressive treatment, more antibiotics, more education
Ways to measure how well Dm is controlled:
blood glucose or tolerance, A1C
What is refractory hypertension:?
can’t get BP down NO MATTER WHAT
What is brittle DM?
no matter what, you can’t get under control, if person is low, then high, etc. more likely to have complications
TF? There might be an inc traumatic ulcers or fibromas in pts w DM.
T
What does a glucometer measure?
capillary blood glucose level
Fasting glucose req no food to be eaten for:
8h
Blood glucose measurements that use capillary blood levels:
Random and fasting plasma and blood glucose (4)
PPG sf:
Postprandial glucose
Normal fasting blood glucose:
100mg/dl or less
What is the glucose tolerance test?
give glucose, serial blood draws over a few hours, plot glucose curve
What does the oral glucose tolerance test reflect?
rate of absorption, tissue uptake and excretion of glucose
Is the oral glucose tolerance test taken while fasting or not?
while fasting
how to take oral glucose tolerance test:
while fasting, give 100gm glucose, venous blood drawn before & at 1, 2 and 3hrs
What would the oral glucose tolerance test for a diabetic show?
inc fasting, inc peak, & delayed return in 2 & 3h samples
How many hours does it take for a pt with DM to dec blood sugar?
4-6h
Pt w DM will have the highest BG level how long after eating sugar?
just after 1h
What does A1C measure?
glucose bound to Hb, control over past 2-3mo
Life span of RBC:
120d
TF? A1C can tell you how well controlled a pts blood glucose is that day.
F. over last 3mo
Nomal A1C value:
4.5-5.8
ADA recommends A1C level to be below:
7%
Over __% is considered poor control for A1C levels:
8%
Prediabetic A1C range:
5.90-6.4%
A1C level for diabetic:
6.5% +
Hemoglobin A1C of 6 = ___ eAG(mg/dl)
125
Hemoglobin A1C of 8 = ___ eAG(mg/dl)
183
Hemoglobin A1C of 10 = ___ eAG(mg/dl)
240
Hemoglobin A1C of 12 = ___ eAG(mg/dl)
298
eAG sf:
estimated average glucose
A1C must be higher than this to dx DM:
6.4
At what A1C level does risk of diabetic retinopathy increase?
6.5%
What is the most sensitive indicator of a high A1C?
retinopathy, dilated eye exam at opthomolagist, sensitive to changes in blood glucose
If a pt has neuropathy they probably have:
early renal involvement
Order of which 2’ issues are likley to present in DM pts:
microalbuminuria, neuropathy, nephropathy, retinopathy
What can happen to preanalytic samples?
can undergo glycolysis
The same sample in a lab for 2d can vary this much:
14%
Is the intraperson A1C test variability high or low?
high
Pop w higher A1C values for given glycemia levels:
African Americans
T?F? A1C tests can have differences bw groups.
T
Criteria for Dm dx for the different tests:
A1C > 6.5%, FPG > 126mg/dl, 2h PG > 200 mg/dl during OGTT, RG >200mg/dl in pt w signs & symptoms of hyperglycemia
OGGT sf:
Oral glucose tolerance test
Prediabetes: IFG:
100-125 (fasting glucose), <140 (2h after eating or 75gm OGTT)
Prediabetes: IGT:
< 100 (fasting glucose), 140-199 (2h after eating or 75gm OGTT)
Diabetes: IGT:
> or = to 126 or > 200 2h after eating or 75gm OGTT, needs confirmatory test OGTT, fasting or metabolic decomp
How much does a 1% drop in A1C reduce the chance of vision loss, kidney failure, and nerve damage?
35%
What’s more important to us in clinic, A1C value or blood sugar at that moment?
blood sugar at that moment
Is Dm curable?
no
Goals for mgmt of DM:
normal glucose, normal w8, control hypertension/ hyperlipidemia, develop a plan that doesn’t dominate a patients life
Meds for DM:
Sulfonylureas, Meglitinides, Biguanides, Glucosidase Inhibitors, thiazolidinediiones
Med for DM that stimulate insulin secretion:
Sulfonylureas, Meglitinides
DM med that decreases glycogenolysis and hepatic glucose production:
biguanides
DM med that dec GI absorption of carbos:
glucosidades inhibitors
DM med that enhances tissue sensitivity to insulin:
thiazolidinediiones
Rapid acting insulin meds:
Novalog, Humalog (3-5h duration)
Short acting insulin meds:
Novalin R, Humalin R (5-8h duration)
Intermediate-acting NHP insulin meds:
Novalin N, Humalin N (12-16h duration)
long-acting insulin meds:
Levemir, Lantis (20-26h duration)
Pre-mixed combo insulin meds:
Humalin 50/50. Novalog 70/30 (10-16h duration)
Drug of choice for Type 2 diabetes:
Metformin
These are often used in conjunction w insulin:
oral meds
TF? If a person takes meds they have Type 1 DM.
F
Which type of DM is more likely to be taking meds?
Type 2 (doesn’t make sense to me)
TF? They only give insulin pumps to pts that can’t control their BG levels well on their own.
F. only pts w good control
New approaches to meds:
oral/ inhaled insulin, injectable hormone analogs, stem cell therapy to create more pancreatic islet cells, antibody therapy
Post-op gastric bypass, intestines produce:
GLUT-1
Is there an inc or dec in inflammation post-op gastric bypass suyrgery?
dec
TF? Gastric bypass can have benefits before weight losss.
T
% relapse after gastric bypass surgery:
30%
Which uses more energy to absorb sugar in the body, intestinal or gastric absorption?
gastric (check) aI assume bs if you have gastric you have both
TF? A pt can immediately become non-diabetic after gastric bypass surgery.
T. seems the stomach is not absorbing the carbs, hormonal influence on small intestines?
What can a prediabetic person do to red risk of developing diabetes by 58%?
lose 5-7% of their weight, exercise 1/2h daily
Complications of metabolic syndrome:
obesity, hypertension, diabetes, hyperlipidemia, low HDL
This is a pro-inflammatory state:
metabolic syndrome, high CRP and other inflammatory mediators
Cardinal symptoms of undiagnosed diabetes:
Polyuriea, Polydypsia, Thirsty, Hungry, Sudden unexplained weight losses/gain
Risk level a a pt w undiagnosed DM:
high risk
What to ask pt w DM:
well controlled? frequency of testing, normal morning reading, readings today & yesterday, take meds & eat today?
Who do we take blood sugar for?
Pt w diabetes who did not test that day
Stress increases:
epi, corticosteroids, glucose and free fatty acid
Stress decreases:
insulin
High levels of this will increase blood glucose:
cortisal
Can stress levels affect how well a pt controls their DM?
yes
Refractory spike in blood glucose is due to:
stress, stimulates glycogenolysis
TF? Significantly increased RBG presents an immediate safety risk.
F, indicator of poor control, detrimental to overall health
Dental care can be continued up to this RBG reading:
400 mg/dl
If a pts RBG is in this range for a few appt they shoudl be refered to thier PCP:
high 300’s
Healthy pt RBG range:
100-150
TF? Pts wo diabetes can become symptomatic at higher lood sugar levels than pts w DM.
F. vice verssa
Give a pt sugar if their RBG reading is:
below 80 mg/dl
Normal fasting glucose:
68-100
Who is symptomatic earlier w changes in blood glucose, diabetic or non-diabetic?
diabetic
Am or Pm appts for diabetics?
am, take meds, eat
If a diabetic pt is shaking are they hypo or hyperglycemic?
hypo
If a pt is taking both injections and oral meds for their DM, do they have Type 1 or Type 2?
Type 2
Do this post-op for diabetic pts:
antibiotics, treat infections aggressively to cure, regain control of DM
Why do diabetics have an inc risk of post-op infection?
delayed wound healing
“Non por oss” means?
nothing by mouth
Sedation pts:
NPO, careful protocols, ie 1/3 usual insulin and intra-op IV glucose
Why might diabetic pts not be able to be tipped back all the way in the dental chair?
GI problems due to meds (glucophage)
Steroid use is related to hypo/ hyper glycemia.
hyper
ASA is related to hypo/ hyper glycemia.
hypo
Low blood sugar symptoms:
sweating, headache, shaking, tired, weak, hungry, personality change
Reasons for hypoglycemia
New or overmedications, missed meals, low carb meals
Increased activity, weight loss, alcohol, early pregnancy, kidney failure, menstrual cycle, gastroparesis
TF? If a pts blood sugar levels are high it is dangerous to give them more sugar.
F.won’t make a difference
Best juice to give to person w low blood sugar:
apple, absorbs faster than orange
Glycemic index of sugar sources:
glucose = 100, sucrose = 65, orange juice = 47, milk = 35
Should diabetics have more frequent recalls?
yes
